Diagnosis of, and differentiation between, primary and secondary causes of hyper- or hypoaldosteronism, management of renal artery stenosis, diagnosis and location of renin secreting tumours & monitoring mineralocorticoid replacement therapy.
The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure.
Renin, which is primarily released by the kidneys, stimulates the formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone from the adrenal cortex.
Renin is a proteolytic enzyme that is released into the circulation primarily by the kidneys. Its release is stimulated by: sympathetic nerve activation (acting via β1-adrenoceptors), renal artery hypotension (caused by systemic hypotension or renal artery stenosis) & decreased sodium delivery to the distal tubules of the kidney.
When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen that undergoes proteolytic cleavage to form the decapeptide angiotensin I.
Recumbent: 1.1 – 2.7 pmol/mL/h. 30 min
Upright: 2.8 – 4.5 pmol/mL/h
Ref range for samples taken randomly: 0.5 – 3.5 pmol/mL/h
Random aldosterone/renin ratio is now the main sample of choice. After strict overnight recumbence take first sample before patient has even sat up. Take second specimen after patient has got out of bed and walked around for 30mins.
Plasma – Lithium Heparin sample is required for this assay. Specimen must be taken straight to laboratory.
Note that spironolactone, calcium channel blockers and ACE inhibitors must be stopped 6 weeks before taking sample.
St James University Hospital